首页> 外文期刊>European Journal of Pharmacology: An International Journal >Baicalin inhibits Staphylococcus aureus-induced apoptosis by regulating TLR2 and TLR2-related apoptotic factors in the mouse mammary glands
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Baicalin inhibits Staphylococcus aureus-induced apoptosis by regulating TLR2 and TLR2-related apoptotic factors in the mouse mammary glands

机译:黄芩苷通过调节小鼠乳腺中的TLR2和TLR2相关的细胞凋亡因子来抑制金黄色葡萄球菌诱导的细胞凋亡

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摘要

Baicalin, the major active constituent of the isolated root of Scutellaria baicalensis, is widely used in China and Southeast Asian countries. Evidence has indicated that baicalin has multiple biological activities, including anti-apoptotic properties. Mastitis is a severe problem in humans and other animals and is characterized by mammary gland cell apoptosis. Staphylococcus aureus (S. aureus) is the major pathogen that causes mastitis. This study was designed to evaluate the protective effects of baicalin on the mammary glands during S. aureus-induced mastitis. In the present study, a mouse model was infected with S. aureus to induce mammary gland injury. Baicalin treatment was administered between 6 and 24 h after infection. Toll-like receptor 2, p53, BAX, BCL-2 and caspase-3 expression were analyzed using qPCR and Western blotting. The results indicated that baicalin significantly attenuated pathological damage and cell death in the mammary glands. Further studies revealed that baicalin down-regulated the expression of Toll-like receptor 2 (TLR2) and the phosphorylation of p53 in the mammary glands after S. aureus-induced mastitis. Baicalin also promoted the expression of BCL-2 at the mRNA and protein levels but inhibited BAX and caspase-3 (CASP-3) cleavage. Baicalin inhibited apoptosis and had protective effects on mammary gland tissues during S. aureus-induced mastitis. These effects were displayed by reductions in TLR2 expression and p53 phosphorylation and the regulation of apoptosis-related factors (BCL-2, BAX and CASP-3) in mammary gland tissues.
机译:黄芩苷,黄芩的隔离根的主要活性成分,广泛应用于中国及东南亚国家。有证据表明,黄芩苷具有多种生物活性,包括抗凋亡特性。乳腺炎是在人类和其他动物的一个严重问题,其特征是乳腺细胞凋亡。金黄色葡萄球菌(金葡菌)是引起乳腺炎的主要病原。这项研究的目的是评估黄芩苷对金黄色葡萄球菌引起的乳腺炎在乳腺的保护作用。在本研究中,小鼠模型被金黄色葡萄球菌感染以诱导乳腺损伤。黄芩苷治疗感染后6小时和24小时之间施用。 Toll样受体2,p53和BAX,BCL-2和胱天蛋白酶-3表达使用qPCR和Western印迹分析。结果表明,黄芩显著在减毒乳腺病理损伤和细胞死亡。进一步研究表明,黄芩下调Toll样受体2(TLR2)和p53的金黄色葡萄球菌引起的乳腺炎后乳腺磷酸化的表达。黄芩也促进BCL-2的表达在mRNA和蛋白质水平,但抑制BAX和caspase-3(CASP-3)裂解。黄芩甙抑制细胞凋亡和对金黄色葡萄球菌诱导的乳腺炎期间乳腺组织的保护作用。这些作用被在TLR2表达和p53磷酸化和凋亡相关因子(BCL-2,Bax和CASP-3)在乳腺组织中的调节减少显示。

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